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Specimen 1300.15 - Bronchopneumonia

Spiel: A 71 year old diabetic was admitted for treatment of depression, which had resulted in severe anorexia (loss of appetite) and weight loss. Shortly after admission, he had an episode of palpitations and low blood pressure, and he developed pneumonia, which improved with antibiotics and physiotherapy. He was managed in the psychiatric Unit, where he had fluctuating states of clouding of consciousness and confusion. His physical condition showed overall deterioration. Three days before his death, he became feverish, with diarrhoea and dehydration. On the day of his death, he had circulatory failure, followed by respiratory and cardiac arrest. The specimen is a section of the left lung and shows extensive consolidation (firmness) of most of the upper lobe. The lower lobe shows the typical patchy appearance of bronchopneumonia.


Question 1

Specimen of the week - Bronchopneumonia

Which organ? The specimen consists of a section of the left lung and shows extensive consolidation of most of the upper lobe. The lesions are confluent and the specimen shows something of the appearance of "lobar" pneumonia. The lower lobe shows the typical patchy appearance of bronchopneumonia.

Question 2

  • Lesion = patchy consolidation

Question 3

  • Pathological processes = bronchopulmonary pneumonia

Question 4

  • Likely series of events
  • Suppurative inflammation
  • Classical stages
    1. congestion (vasodilation produces exudation in the alveoli due to inflammation; lung appears heavy, red and foggi)
    2. red hepatisation (alveoli filled with neutrophils and fibrinous exudate - a fibrinous suppurative exudate - causes the lung to become solid, like the liver. Congested with blood. Red due to red blood cells)
    3. grey hepatisation (alveoli appear grey after red blood cells lyse)
    4. resolution (exudate is liquified and phagocytosed, mainly by alveolar macrophages, and thencoughed out, leading to a complete return to normal structure and function) (NOT IN THIS CASE!)

Question 5

Clinical manifestations

  • Symptoms:
    • chills, rigors (shaking), productive cough (might look rusty due to exit of RBCs in alveoli), pleuritic chest pain (spread of inflammation to pleura surface)
  • Signs:
    • fever, tachypnoea, dullness to percussion, crepitations and/or bronchial breathing (harsh upper airway sounds are not interrupted by air entering alveolar spaces), pleural friction rub
      • fever, tachypnoea and tachycardia is pneumonia until proven otherwise
  • Laboratory findings:
    • neutrophil leucocytosis, hypoxaemia, sputum with PMN and causative organism found on Gram stain

Lobar pneumonia 1048.10 Lobar pneumonia (Lt upper lobe) and Bronchopneumonia 1300.15 have the same clinical manifestations

  • Severe fever with rigors or shivering attacks
  • Cough with ‘rusty’ blood-stained sputum (red hepatisation)
  • Difficulty breathing
  • Pleurisy; characterized by sharp pain on coughing or on deep inspiration and pleural friction rub
  • Septicaemia with high temperature
  • Crackles (crepitations) on auscultation of affected areas

Wikipedia In bacterial pneumonia, invasion of the lung parenchyma by bacteria produces an inflammatory immune response. This response leads to a filling of the alveolar sacs with exudate. The loss of air space and its replacement with fluid is called consolidation. In bronchopneumonia, or lobular pneumonia, there are multiple foci of isolated, acute consolidation, affecting one or more pulmonary lobes. Although these two patterns of pneumonia, lobar and lobular, are the classic anatomic categories of bacterial pneumonia, in clinical practice the types are difficult to apply, as the patterns usually overlap. Bronchopneumonia (lobular) often leads to lobar pneumonia as the infection progresses. The same organism may cause one type of pneumonia in one patient, and another in a different patient. From the clinical standpoint, far more important than distinguishing the anatomical subtype of pneumonia, is identifying its causative agent and accurately assessing the extent of the disease.

Kumar's response when asked whether bronchopneumonia and lobar pneumonia have different manifestations

  • In all likelihood, they won't. Bacterial pneumonia typically presents with cough and fever, a variable amount of breathlessness, and possibly haemoptysis. These will be no different for classical lobar vs bronchopneumonia. In fact far too much attention is given to classical lobar pneumonia, which although common in the pre-antibiotic era, is now rarely seen in its full-blown form because of antimicrobial therapy. In any case it really only developed in otherwise healthy young adults. So if there is a clinical difference, it will be with respect to pre-existing disease which may have predisposed to the development of bronchopneumonia.
  • These days, if consolidation appears radiologically to be lobar, it usually turns out to be confluent bronchopneumonia. There is in any case so much overlap between the two morphological patterns that the distinction is relatively unhelpful -- what matters is the causative organism and its antimicrobial sensitivity.

Question 6


(Mostly associated with typical bacteria pneumonia)

  • Abscess - localised collection of pus in an organ or tissue
    • Clinically:Onset of symptoms is often gradual, but in necrotizing staphylococcal or gram-negative bacillary pneumonias patients can be acutely ill. Cough, fever with shivering and night sweats are often present. Cough can be productive with foul smelling purulent sputum (≈70%) or less frequently with blood (i.e. hemoptysis in one third cases). Affected individuals may also complain of chest pain, shortness of breath, lethargy and other features of chronic illness. Patients are generally cachectic at presentation. Finger clubbing is present in one third of patients. Dental decay is common especially in alcoholics and children. On examination of chest there will be features of consolidation such as localised dullness on percussion, bronchial breath sound etc.
  • Empyema - pus in an organ or cavity (e.g. pleural cavity)
    • Symptoms of pleural empyema may vary in severity. Typical symptoms include: cough, fever, chest pain, sweating and shortness of breath. Clubbing may be present in cases of a chronic nature. There is a dull percussion note and reduced breath sounds on the affected side of the chest. Other diagnostic tools include a blood white cell count, chest x-ray, CT scan, and ultrasonography.
  • Disseminated infection
    • In addition to symptoms related to the provoking infection, sepsis is characterized by presence of acute inflammation present throughout the entire body, and is, therefore, frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower-than-average temperature, and vomiting[citation needed]. The modern concept of sepsis is that the host's immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by an elevated heart rate (above 90 beats per minute), high respiratory rate (above 20 breaths per minute or a partial pressure of carbon dioxide in the blood of less than 32), abnormal white blood cell count (above 12,000, lower than 4,000, or greater than 10% band forms) and elevated or lowered body temperature, i.e. under 36 °C (97 °F) or over 38 °C (100 °F). Sepsis is differentiated from SIRS by the presence of a known or suspected pathogen. For example SIRS and a positive blood culture for a pathogen indicates the presence of sepsis. However, in many cases of sepsis no specific pathogen is identified.

This immunological response causes widespread activation of acute-phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter-regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.

    • Meningitis (nuchal rigidity, headache, sudden high fever, altered mental status, photophobia, phonophobia), septic arthritis (rapid onset of jt pain; A number of factors should increase one's suspicion of the presence of an infection. In children these are: fever > 38.5 C, non-weight-bearing, serum WBCs > 12 x 10^9, ESR > 40 mm/hr, CRP > 20 mg/dL), infective endocarditis
    • Septic shock and muliple organ failure (most likely cause of death)
      • In humans, septic shock has a specific definition requiring several criteria for diagnosis:
First, SIRS (systemic inflammatory response syndrome) must be met by finding at least any two of the following:

Tachypnea (high respiratory rate) > 20 breaths per minute, or on blood gas, a PCO2 less than 32 mmHg signifying hyperventilation.

White blood cell count either significantly low, < 4000 cells/mm³ or elevated > 12000 cells/mm³.
Heart rate > 90 beats per minute
Temperature: Fever > 38.5 °C (101.3 °F) or hypothermia < 35.0 °C (95.0 °F)
Second, there must be sepsis and not an alternative form cause of SIRS. Sepsis requires evidence of infection, which may include positive blood culture, signs of pneumonia on chest x-ray, or other radiologic or laboratory evidence of infection
Third, signs of end-organ dysfunction are required such as renal failure, liver dysfunction, changes in mental status, or elevated serum lactate.
Finally, septic shock is diagnosed if there is refractory hypotension (low blood pressure that does not respond to treatment). This signifies that intravenous fluid administration alone is insufficient to maintain a patient's blood pressure from becoming hypotensive.
  • wikipedia:Respiratory failure (particularly in widespread pneumonia)
  • Organisation of exudate (if you can't remove it, then scarring can produce permanent reduction in surface area available for gas exchange) (restrictive pattern of lung disease)